Endocrine Pathology Flashcards
Organs of the Endocrine System
Pituitary gland • Thyroid gland • Parathyroid gland • Adrenal gland • Pancreas
Hypothalamus
— coordinating center
- Temperature regulation
- Food intake
- Thirst and water intake
- Sleep and awake patterns
- Emotional behavior
- Memory
Hypothalamic-pituitary axis
Involves the Thyroid gland, Adrenal glands, and Gonads
CRH (hypothalamus) –> ACTH –> cortisol (cortisol negatively feedbacks on both CRH and ACTH)
- Influences growth
- Milk production
- Water balance
General Terms in Endocrine disorders
Hypo-secretion — Hormone deficiency
Hyper-secretion — Hormone excess
Tumors — benign or malignant
Major Pituitary Gland Disorders
Acromegaly,
Diabetes insipidus,
Hypopituitarism,
Pituitary tumor
Major Anterior Pituitary Hormones
ACTH (adrenal cortex) salt and water balance, BP, blood sugar levels, muscle
strength, mood, immune system, heart, lungs, blood vessels, nervous system
o TSH = thyroid metabolism
o GH =strong bones, lean muscle, protein production
o MSH = smooth firm skin (MSH)
o FSH, LH (gonadotropins) = testes and ovaries for sex characteristics and libido
o Prolactin = breast milk production
Major Posterior Pituitary Hormones
ADH (kidney) =water retention, blood pressure
Oxytocin = muscle contraction (breast)
*note that the posterior pituitary does not PRODUCE hormones but stores hormones made in the hypothalamus
List of Pituitary Hormones
TSH — Thyroid stimulating hormone (thyrotropin)
- PRL — prolactin
- ACTH — adrenocorticotropic hormone (corticotropin)
- GH — growth hormone (somatropin)
- FSH — follicle stimulating hormone
- LH — luteinizing hormone
- MSH — melanocyte stimulating hormone
Stimulatory releasing factors (hypothalamus)
- TRH — thyrotropin releasing hormone
- CRH — corticotropin releasing hormone
- GHRH —growth hormone releasing hormone
- GnRH — gonadotropin releasing hormone
Inhibitory hypothalamic influence
- PIF — prolactin inhibiting factor
- GIH — growth inhibiting factor (somatostatin)
Hyperpituitarism — tumors
- Excess
- Adenoma, hyperplasia, carcinoma of the anterior pituitary
Hypopituitarism — small injury
- Deficit
- Destructive processes, ischemic injury, surgery, radiation, inflammatory reactions and
nonfunctional adenomas
Types of Pituitary Tumors
Adenomas (most common)
Proclatinomas
Non-functional Pituitary Adenomas
tend to be larger than those that secrete hormone
- Start out slow growing and don’t have any symptoms
- But eventually become very large
- Compress everything around it
- Thus symptoms in the beginning may not be associated with a tumor!
Compresses the optic nerve –> tunnel vision, headaches, etc
Tunnel vision = bilateral (always) compression of the optic nerve, so no peripheral vision
Secreting Pituitary Adenomas
Can effect the following cells and cause these syndromes
Lactoproh > Prolactin > Galactorrhea, Amenorrhea, Infertility
Somatotroph > GH and Prolactin > Gigantism and Acromegaly
Corticotroph > ACTH > Cushing syndrome and Nelson syndrome
Thyrotroph > TSH > Hyperthyroidism
Gonadotroph > FSH, LH > Hypogonadism and Hypopituitarism
most common alterations in pituitary adenomas
G-protein mutations
- G-proteins play a critical role in signal transduction
- G-protein hyperactivity
Gigantism
Hyperpituitaryism
Adenoma appears in children BEFORE the epiphyses have closed
Increase in body size with disproportionally long arms and legs
Acromegaly
Excessive secretion of growth hormone AFTER BONESN ALREADY FORMED (adulthood)
- Excessive growth of hands, legs, soft tissues
- Protruding jaws
- Enlargement of organs
Compression from an adenoma will create different problemsin different parts of the body - Certain body parts can’t expand anymore!!
Common signs and symptoms:
- Headaches, vision changes, hypertension, heart enlargement (from greater demand),
pulmonary problems, glucose intolerance (T2D associated with it), pain in joints,
difficulty with mobility
- Main characteristics are in the extremities
- Chief complaint at dentist = “my profile is changing and my teeth are shifting/getting
more spaces”
o Teeth get more spacing because the jaw is growing
Effects of Excess Growth Hormone in the body
Gonadal dysfunction
Diabetes mellitus
Muscle weakness
Hypertension
Arthritis
Congestive heart failure
Increased risk of GI cancer
GH regulates IGF, which is primarily secreted in the liver
- This will affect different parts of the body depending
on when the problem occurred
- Specifically, it affects bone metabolism and growth
Corticotroph adenomas
Secrete ACTH
Main characteristics:
- Cushing syndrome
- Hyperpigmentation
Cushing syndrome
Excessive production of ACTH — Cushing disease
The various causes of Cushing’s syndrome:
- 1. A pituitary tumor makes ACTH, which stimulates production of cortisol by the adrenal
gland. High cortisol levels inhibit CRH secretion and ACTH secretion from normal
pituitary cells
- 2. Ectopic ACTH secretion —a non-pituitary tumor makes ACTH, which stimulates
production of cortisol by the adrenal gland. High cortisol levels inhibit CRH secretion and
ACTH secretion from normal pituitary cells
- 3. Primary adrenal disease —adrenal glands independently make too much cortisol.
High cortisol levels inhibit CRH secretion and ACTH secretion from normal pituitary cells
Key
Most common is anterior lobe pituitary adenoma
Macroadenomas and microadenomas
Functioning – associated with endocrine signs and symptoms
Non-functioning — mass effects, visual disturbances
- Slow growing and can get very big
- First symptoms will be visual disturbances and headaches
Hypopituitarism
Low secretion of hormones Diseases of the hypothalamus or of the pituitary - Destructive disorders - Tumors/mass lesions - Traumatic brain injury - Surgery or radiation - Apoplexy - Ischemic disorders and Sheehan syndrome - Cyst - Hypothalamic lesions - Inflammatory disorders and infections
Sheehan syndrome
due to ischemic necrosis
- During pregnancy gland size increases
- If obstetrical hemorrhage occurs, relative hypoxia compromises gland
- Can also occur in DIC, sickle cell, meningitis, inflammatory disorders, and sarcoidosis
o Sickle cells can obstruct blood vessels
Anterior Pituitary Hypofunction
Clinical manifestations GH deficiency — growth failure LH and FSH —amenorrhea and infertility PRL — failure of postpartum lactation TSH and ACTH — hypothyroidism and hypoadrenalism
Diabetes Insipidus
Insufficient production of Anti-diuretic hormone
- Excessive thirst and excretion of large amounts of urine
- Thirst, blurred vision, dehydration, extreme urination, fever, diarrhea, and vomiting
Etiology — Central diabetes insipidus
- Pituitary surgery, Craniopharyngioma, Post-traumatic head injury, Congenital malformations, Genetic mutations, Autoimmune disorders, Medications (phenytoin),Cerebrovascular accident (CVA, stroke)
Etiology – Nephrogenic diabetes insipidus
- Medications (long term lithium, cisplatin, propoxyphen)
- Chronic diseases — sickle cell anemia, renal sarcoidosis, poorly controlled diabetes
mellitus
Thyroid Gland
Abnormalities in the anterior pituitary or the thyroid gland itself can result in abnormal thyroid hormone production
Thyrotropin releasing hormone (from hypothalamus) >> thyroid stimulating hormone (from anterior pituitary) >> thyroid hormone (from thyroid gland, has direct effect on gland)
3 hormones —T4, T3, Calcitonin Needed for: - Growth and maturation of tissues - Cell respiration - Energy expenditure
Function of Thyroid Hormones
T4 (thyroxine) - Oxygen consumption, cholesterol degradation, GI motility, bone
turnover, mental alertness, carb metabolism
T3 (triiodothyronine) - Heart contractility/contraction rate (increased)
Calcitonin - Skeletal remodeling, absorption of calcium, resorption of bone by osteoclasts
Hyperthyroidism
Iodine-induced hyperthyroidism
Secondary — pituitary adenoma (rare)
Clinical manifestations
- Metabolic rate
o Heart will be affected: Tachycardia and palpitations as a compensatory mechanism, but this can
lead to cardiomegaly/ Prone to arrhythmias because the heart has to work more
o Heat intolerance, weight loss, etc
o Problems with sympathetic function of GI tract (Hypermotility, malabsorption, diarrhea)
- **Malabsorption also leads to low levels of vitamins, especially VB12
- **May have problems with coagulation because of lack of vitamin K
o Weight loss even if eating a lot
- Skeletal system
o Decreased bone mass, thus prone to osteoporosis
Grave’s disease
Autoimmune disease
o Thyroid overactive»_space; Excessive amount of thyroid hormones
o Auto-antibodies to the TSH-receptor, stimulating hormone synthesis and secretion, and thyroid growth
Graves Disease is the most common cause of endogenous hyperthyroidism
- Diffuse enlargement of the gland
- Exophthalmos»_space; due to accumulation of connective tissue behind the eyes
- Long continued palpitations
- Peak 20 and 40 years of age
- Autoimmune
Hyperthyroidism —thyrotoxicosis
Thyrotoxicosis
- Excess T3 and T4 in the bloodstream
- Etiology — Ectopic thyroid tissue, multinodular goiter, thyroid adenoma, subacute
thyroiditis, ingestion of thyroid hormone, pituitary disease
- Increased metabolic activity by excessive hormone secretion increases heart rate, pulse
- Congestive heart failure may occur
- Dyspnea, Reduction of vital capacity
- GI ulcers
- RBC mass is enlarged to carry additional oxygen
- Requirements for B12 and folic acid are increased
Thyrotoxic Crisis
- Untreated or incompletely treated thyrotoxicosis
- Rare complication — marked tachycardia, arrhythmia, pulmonary edema, and HF
- Precipitating factors — infection, trauma, surgical emergencies
Hypothyroidism
Slow metabolism
In utero –> Cretinism
In adults –> Myxedema
Primary disease —Failure of the thyroid gland to produce T3 and T4; Autoimmune or damage to the thyroid gland
Secondary disease —thyroid gland is normal, but pituitary gland does not secrete TSH
Tertiary disease — failure of the hypothalamus to secrete TRH
Hashimoto’s thyroiditis
Inflammation of the thyroid gland
Autoimmune disorder
Symptoms
- Fatigue
- Muscle weakness
- Weight gain
- Bradycardia
- Thick tongue
- Eyelid edema
- Goiter
Potential causes
- Genetic predisposition
- Current autoimmune disorder
- Pregnancy or postpartum trigger
- Excessive iodine intake
- Viral of bacterial infection
- Menopause
- Drugs
Myxedema
Diminished production of thyroxin
Mucoprotein and extracellular fluid is deposited in the intracellular space, especially in dermal
connective tissue edematous appearance
- Not true edema because it’s not fluid accumulation
Decreased metabolism
Extreme fatigue
Low pulse rate
Low BP
Puffy face
Non-pitting edema
*- Vs. Pitting edema usually for cardiovascular disease; Usually bilateral, lower extremity edema
Cretinism
Dwarfism
Coarse dry skin
Deficient hair and teeth
Retarded skeletal growth
Acute infectious thyroiditis
Viral or bacterial infection
Could be related to the pharynx or upper respiratory tract
Only causes transient hypothyroidism —goes away!
Thyroiditis
Painful gland Variable enlargement Inflammation and hyperthyroid are transient 2-6 weeks High serum T4 and T3 with low TSH 6-8 weeks normal function returns NSAIDS to treat
Thyroid Cancer
Papillary carcinoma (85% of cases)
- Risk increases with prior exposure to radiation
o This is why we use the thyroid collar when taking x-rays! The thyroid is very
sensitive to radiation!!!!!!!!
Follicular carcinoma (5-15% of cases)
Anaplastic (undifferentiated) carcinoma (<5% of cases)
Medullary carcinoma (5% of cases)
Papillary carcinoma
Presents as a thyroid nodule
Rapid nodular growth
Multifocal
Hoarseness or vocal cord paralysis
Ipsilateral cervical nodes
Age at diagnosis better if between 25-40
Poorer prognosis if tumors are large
Risk factors —radiation, family history of thyroid cancer
- Exposure to ionizing radiation in childhood
- 1 st degree relative with thyroid carcinoma or family history of thyroid cancer syndrome
Parathyroid hormone (PTH)
Secreted by the parathyroid glands by their chief cells; Parathyroid gland regulates calcium homeostasis
Increases the renal tubular reabsorption of calcium, conserving free calcium
Increases the conversion of vitamin D to its active di-hydroxy form in the kidneys
Increases urinary phosphate excretion, lowering serum phosphate levels
Augments GI calcium absorption
Hyperparathyroidism
Primary — Adenoma or hyperplasia
Secondary — compensatory mechanism in response to hypocalcemia
Tertiary — persistent hypersecretion of PTH (even after prolonged hypocalcemia, after renal transplant)
